For example, in AD, tau lesions accumulate in a defined spatiotemporal pattern: first, appearing in the transentorhinal cortex, then, spreading to anterior hippocampus and adjacent neocortex, and, finally, invading the primary sensory cortex.[36] Missorted tau at somatodendritic compartments can be released into the extra‐neuronal space via secretion or other mechanisms.[37] These findings suggest that intra‐neuronal tau proteins, after aggregation, may obtain prion‐ or β‐amyloid‐like properties. The gene discussed is MAPT; the disease is Alzheimer disease.